Unique regulation of SclB -: a novel collagen-like surface protein of Streptococcus pyogenes
Unique regulation of SclB -: a novel collagen-like surface protein of Streptococcus pyogenes
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DOI：
10.1046/j.1365-2958.2001.02493.x
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发表时间：
2001-06-01
影响因子：
3.6
通讯作者：
Björck, L
中科院分区：
文献类型：
--
作者：
Rasmussen, M;Björck, L
在含有所谓的编码重复序列（CR）的位点处的滑动链错配可以导致革兰氏阴性菌中表面蛋白的相变化。这种机制，被认为有助于毒力，迄今尚未确定在革兰氏阳性细菌。在革兰氏阳性人类病原体化脓性链球菌的基因组中，我们在编码新的胶原样表面蛋白（表示为SclB）的开放阅读框（ORF）的推定信号序列内鉴定了五核苷酸CR。在12 S.在化脓性链球菌菌株中，sclB基因中的CR数目从3个变化到19个，使得起始密码子在4个菌株中与下游ORF在框内，在8个菌株中在框外。与抗SclB抗体反应的蛋白质只能从三个菌株中溶解，所有菌株都含有完整的sclB基因。在同一M血清型的菌株中观察到CR数量的变化，并发生在S生长期间。化脓性链球菌在新鲜人血中，而不是在培养基中。SclB蛋白具有高变的N-末端部分、胶原样中心部分和含有LPXTGX基序的典型细胞壁分选序列。SclB与胶原样SclA相关，并且与SclA一样参与S.将化脓性细菌转化为人体细胞然而，已知上调sclA和几个编码S.化脓性链球菌，下调sclB转录。这一观察结果和SclB通过滑动链错配而改变相位的潜力强调了这种新的S.化脓菌表面蛋白
Slipped-strand mispairing at sites containing so-called coding repeats (CRs) can lead to phase variation of surface proteins in Gram-negative bacteria. This mechanism, believed to contribute to virulence, has so far not been identified in a Gram-positive bacterium. In the genome of the Gram-positive human pathogen Streptococcus pyogenes, we identified pentanucleotide CRs within a putative signal sequence of an open reading frame (ORF) encoding a novel collagen-like surface protein, denoted SclB. In 12 S. pyogenes strains, the number of CRs in the sclB gene varied from three to 19, rendering the start codon in frame with the downstream ORF in four strains and out of frame in eight strains. A protein reacting with anti-SclB antibodies could only be solubilized from three strains, all containing an intact sclB gene. Variations in the number of CRs were observed within strains of the same M serotype and occurred during growth of S. pyogenes in fresh human blood, but not in medium. The SclB protein has a hypervariable N-terminal part, a collagen-like central part and a typical cell wall sorting sequence containing the LPXTGX motif. SclB is related to the collagen-like SclA and is, like SclA, involved in the adhesion of S. pyogenes bacteria to human cells. However, the Mga protein, known to upregulate sclA and several additional genes encoding virulence factors of S. pyogenes, downregulates sclB transcription. This observation and the potential of SclB to phase vary by slipped-strand mispairing emphasize the unique regulation of this novel S. pyogenes surface protein.